Myotonia was induced in rats by 2,4-D administration. Creatine kinase and acid phosphatase activities were determined in muscles of different function and metabolism. Based on data from the literature and the present results a mechanism is proposed concerning the metabolic alterations occurring in this type of myotonia. The prolonged contraction and hypoxia damage the oxidative energy-producing system in skeletal muscle. This is reflected in decreased LDH-1, MDH, and CK activities. Under these circumstances the ∼P supply of the muscle tissue is ensured by the enhanced anaerobic glycolytic rate appearing due to regulatory changes. The activated LDH-5 can ensure the continuity of glycolysis. According to the results, the metabolic changes are more pronounced in the white muscle. In the heart muscle the decreased activity of CK and increased activity of acid phosphatase can be interpreted as a primary, toxic effect.
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